The major emphasis of the laboratory continues to include: determination of the biochemical mechanisms and points of pharmacologic modulation in the immunologic release of chemical mediators of immediate hypersensitivity such as histamine, slow reacting substance of anaphylaxis (SRS-A), platelet activating factor(s) (PAF), and eosinophil chemotactic factor of anaphylaxis (ECF-A); physicochemical characterization and functional assessment of the mediators, SRS-A, PAF and ECF-A; delineation of the interrelationships and controls of the Hageman factor dependent sequences of coagulation, fibrinolysis, and kinin generation; recognition and measurement of new factors which modulate polymorphonuclear cell function such as the active site chemotactic factors, kallikrein and plasminogen activator, and the neutrophil immobilizing factor (NIF); and the further isolation and definition of proteins involved in the alternate pathway to complement activation such as factor D and its precursor. Within the past five years five new principles have been recognized, the eosinophil chemotactic factor of anaphylaxis (ECF-A), the Hageman factor fragments, the plasminogen proactivator, the neutrophil immobilizing factor (NIF), and factor D, largely because diverse systems of inflammation are considered in an integrated fashion. This emphasis will continue and be aided by the availability of purified plasma proteins of the various effector systems, well characterized chemical mediators, precise assays for both, and discriminating in vitro models for analysis of the formation and action of chemical mediators. BIBLIOGRAPHIC REFERENCES: Austen, K.F., Lewis, R.A., Wasserman, S.I., and Goetzl, E.J.: Generation and release of chemical mediators of immediate hypersensitivity in human cells. In: NEW DIRECTIONS IN ASTHMA, M. Stein, ed., The American College of Chest Physicians, Park Ridge, Illinois, p. 187, 1975. Austen, K.F., and Orange, R.P.: Bronchial asthma: The possible role of the chemical mediators of immediate hypersensitivity in the pathogenesis of subacute chronic disease. Amer. Rev. Resp. Dis. 112:423, 1975.